Chronic Pelvic Pain in Women: Endometriosis Consideration

By: Steven McCarus. MD

Chronic pelvic pain (CPP) affects millions of women and is defined as non-cyclic pelvic pain lasting six months or longer. It is a complex condition that can significantly impact physical health, emotional well-being, and quality of life. Among the many causes of CPP, endometriosis remains one of the most common and underrecognized contributors.

Endometriosis occurs when endometrial-like tissue grows outside the uterus, leading to inflammation, fibrosis, and adhesions. These lesions can involve the ovaries, pelvic peritoneum, uterosacral ligaments, bowel, bladder, and, in some cases, extra-pelvic sites. The resulting inflammatory environment and nerve involvement make endometriosis a major driver of chronic pelvic pain, often presenting as dysmenorrhea, deep dyspareunia, non-cyclic pelvic pain, and pain with bowel or bladder function.

One of the challenges in managing endometriosis-related pelvic pain is the poor correlation between disease burden and symptom severity. Even minimal disease can cause severe pain due to neurogenic inflammation and central sensitization, while extensive disease may be relatively asymptomatic. This underscores the importance of listening to patients’ symptoms rather than relying solely on imaging or surgical findings.

Diagnosis is frequently delayed, with many women experiencing years of symptoms before receiving appropriate care. While imaging can be helpful in identifying advanced disease, endometriosis remains a clinical diagnosis, and minimally invasive laparoscopy plays a key role when medical therapy fails or symptoms persist.

Effective management requires a multidisciplinary, individualized approach, combining hormonal therapies, pain modulation strategies, pelvic floor physical therapy, and, when indicated, minimally invasive surgical excision. The goal is not only pain relief but also long-term improvement in function and quality of life.

Recognizing endometriosis as a central cause of chronic pelvic pain allows clinicians to intervene earlier, validate patient experiences, and provide more targeted, compassionate care for women living with this often-debilitating condition.

Treatment Considerations

Treatment of chronic pelvic pain associated with endometriosis is most effective when individualized and multidisciplinary. First-line management often includes hormonal therapies such as combined oral contraceptives, progestins, or GnRH analogs, aimed at suppressing ovulation and reducing inflammatory activity. Adjunctive pain-modulating therapies may help address central sensitization.

For patients with persistent symptoms despite medical management, minimally invasive surgical excision of endometriosis can play a critical role, particularly when performed by experienced surgeons. Excision, rather than ablation, is associated with improved pain relief and functional outcomes in appropriately selected patients.

Equally important is addressing coexisting pain generators, including pelvic floor dysfunction, bladder pain syndrome, and irritable bowel syndrome. Pelvic floor physical therapy, psychological support, and lifestyle-based interventions are key components of comprehensive care.

Ultimately, successful treatment extends beyond lesion removal—it focuses on restoring function, validating patient experiences, and improving long-term quality of life. Early recognition and thoughtful management of endometriosis can significantly alter the trajectory of chronic pelvic pain for many women.

GnRH Therapy: Agonists vs Antagonists in Endometriosis-Related Pelvic Pain

Gonadotropin-releasing hormone (GnRH) therapies play an important role in the medical management of endometriosis-associated chronic pelvic pain by suppressing ovarian estrogen production. These agents are particularly useful for patients with moderate to severe symptoms who do not respond adequately to first-line hormonal therapy.

GnRH agonists, such as leuprolide acetate (Lupron®), work by initially stimulating pituitary GnRH receptors, leading to a transient estrogen “flare,” followed by receptor downregulation and profound hypoestrogenism. While effective in reducing endometriosis-related pain, this initial flare can temporarily worsen symptoms. Long-term use is limited by hypoestrogenic side effects, including vasomotor symptoms, vaginal dryness, mood changes, and bone mineral density loss. For this reason, add-back therapy with low-dose estrogen and/or progestin is recommended to improve tolerability and allow extended treatment when needed.

In contrast, GnRH antagonists directly and competitively block GnRH receptors, resulting in rapid suppression of gonadotropins without an initial flare effect. Oral antagonists offer the advantage of flexible dosing and quicker onset and offset of action. This allows for symptom control while potentially minimizing side effects through partial estrogen suppression. As with agonists, hypoestrogenic symptoms can occur, and add-back therapy may be required depending on dose and duration.

When choosing between GnRH agonists and antagonists, clinicians must consider symptom severity, prior treatment response, side-effect tolerance, patient preference, and reproductive goals. Both therapies are effective for pain suppression but do not eradicate disease, emphasizing their role as symptom-management tools rather than definitive treatment.

Used thoughtfully, GnRH-based therapies can provide meaningful pain relief, serve as a bridge to surgery, or help delay surgical intervention while maintaining quality of life.